Lichen Sclerosus

Table of Contents

  1. What is Lichen Sclerosus?
  2. Epidemiology: Who Gets Lichen Sclerosus?
  3. Pathogenesis: Autoimmunity and ECM1 Autoantibodies
  4. Vulvar Lichen Sclerosus: Symptoms and Progression
  5. Genital LS in Men: BXO and Phimosis
  6. Extragenital Lichen Sclerosus
  7. Squamous Cell Carcinoma Risk
  8. Diagnosis: Clinical Recognition and Biopsy
  9. Topical Corticosteroids: First-Line Treatment in Guidelines
  10. Second-Line and Surgical Treatments
  11. Monitoring and Long-Term Follow-Up
  12. Key Research Papers
  13. Connections
  14. Featured Videos

What is Lichen Sclerosus?

Lichen sclerosus (LS) is a chronic inflammatory skin disease. A 1999 Lancet review describes it as most common in adult women but also seen in men and children; any skin site may be affected (and, rarely, the oral mucosa), but it is most common in the anogenital area, where it causes intractable itching and soreness. The same review notes that a wart virus and the spirochaete Borrelia have been suggested as infective triggers but not substantiated (PubMed PMID: 10348006). A 2013 review describes LS in men and women as usually a scarring, chronic progressive or relapsing and remitting, lifelong condition (PubMed PMID: 23329078).

A 2016 review describes LS as thought to be underdiagnosed and undertreated, and states that untreated LS is associated with more scarring and a raised risk of cancer in the genital area (PubMed PMID: 27232363). In a Sydney cohort of 507 women, the mean duration of symptoms before presentation was 5.0 years (range 0.1–40) (PubMed PMID: 26070005).

Epidemiology: Who Gets Lichen Sclerosus?

The exact prevalence is uncertain, partly because LS can occur without symptoms (PubMed PMID: 10348006). The 2018 British Association of Dermatologists (BAD) guideline states: “The estimated prevalence in adult female patients is up to 3%, and 0·07% in men” (PubMed PMID: 29313888). In one US general gynecology practice, 28 of 1,675 consecutive patients (1.7%) had biopsy-proven vulvar LS; of the 19 newly diagnosed women, 11 had no symptoms, and the authors concluded that at least one third of patients may be asymptomatic (PubMed PMID: 16130842). In a Dutch pathology registry, the incidence of LS rose from 7.4 to 14.6 per 100,000 woman-years between 1991 and 2011 (PubMed PMID: 27257093). The 2013 review reports that affected female patients clearly outnumber male patients, with onset peaking in prepubertal children, in postmenopausal women and in men in their fourth decade, and cites a prevalence of 0.1% in premenarchal girls (PubMed PMID: 23329078).

The BAD guideline states that “an increased incidence of tissue‐specific antibodies and associations with other autoimmune diseases, especially thyroid disease, have been documented in women with LS, but this is not the case in men” (PubMed PMID: 29313888). A 2026 meta-analysis of 11 observational studies found LS associated with morphoea (odds ratio 33.33), lichen planus (6.30), vitiligo (4.28), alopecia areata (3.89), psoriasis (1.96) and autoimmune thyroid disease (OR 1.97, 95% CI 1.35–2.88), and with gastrointestinal autoimmune disorders such as coeliac disease; no significant association was found with systemic lupus erythematosus or ulcerative colitis (PubMed PMID: 41725174). Older single-centre studies summarized in the 2013 review reported autoimmune thyroiditis in 12% of 350 women with LS, thyroid disease in 16% of an LS cohort versus 8% of controls, and thyroid disease in 30% of 211 women with biopsy-proven LS (PubMed PMID: 23329078).

Pathogenesis: Autoimmunity and ECM1 Autoantibodies

The cause of LS is unknown. The 1999 review describes an apparent genetic susceptibility and a link with autoimmune mechanisms (PubMed PMID: 10348006); the 2013 review describes recent findings as pointing “towards an autoimmune-induced disease in genetically predisposed patients and further away from an important impact of hormonal factors” (PubMed PMID: 23329078).

ECM1 Autoantibodies

In a 2003 Lancet study, serum from 64 of 86 people with LS (74%) reacted with recombinant extracellular matrix protein 1 (ECM1), compared with 6 of 85 healthy controls (7%). The authors described this as evidence for a specific humoral immune response to ECM1 in LS (PubMed PMID: 12867112). The 2013 review notes that ECM1 autoreactivity was more likely with disease lasting more than a year or more extensive disease, suggesting a role in progression rather than initiation, and that some authors regard ECM1 autoimmunity as possibly an epiphenomenon; autoantibodies to basement membrane zone components have also been reported (PubMed PMID: 23329078).

Lymphocyte-Mediated Inflammation

A 2005 histopathology review describes vulvar LS as a lymphocyte-mediated chronic skin disease in which the lymphocytic infiltrate can be sparse or dense (PubMed PMID: 16178888). The histological features are described under Diagnosis below.

Hormonal and Genetic Factors

The 2013 review reports that serum dihydrotestosterone was significantly decreased in untreated vulvar LS and that androgen receptors are lost from lesional skin as the disease progresses. Topical testosterone, once used on the basis of those findings, has been abandoned for lack of evidence of effectiveness (PubMed PMID: 23329078). In the 2011 Cochrane review, four trials found no significant benefit for topical testosterone, dihydrotestosterone or progesterone, and topical testosterone used as maintenance after clobetasol propionate worsened symptoms (PubMed PMID: 22161424). HLA-DQ7 occurs more often in both women and men with LS (PubMed PMID: 23329078), and about 10% of patients have other family members with the condition (PubMed PMID: 27232363). The 1999 review describes the Koebner phenomenon (LS appearing in skin already scarred or damaged) and suggests trauma and injury as possible triggers in genetically predisposed people (PubMed PMID: 10348006); the 2013 review adds that LS can recur in grafts and circumcision scars (PubMed PMID: 23329078). In men, the London series implicated urinary contact in the pathogenesis (PubMed PMID: 21707769).

Vulvar Lichen Sclerosus: Symptoms and Progression

The 1999 review describes LS as most common in adult women (PubMed PMID: 10348006).

Primary Symptoms

Itch is listed as the most common presenting symptom of LS in the 2013 review, which also describes dyspareunia (painful intercourse) and, from erosions or fissures, pain, soreness and dysuria (PubMed PMID: 23329078). Some women have no symptoms: in the US gynecology practice study, 11 of 19 newly diagnosed women were asymptomatic, and 7 of those 11 already had scarring of the clitoral prepuce or resorption of the labia minora (PubMed PMID: 16130842).

Morphological Findings

The EuroGuiderm guideline describes the first signs as redness and oedema, typically followed by whitening of the genital skin, with fissuring, scarring, shrinkage and fusion of structures sometimes following (PubMed PMID: 38822578). The 2013 review describes fragility as a hallmark of LS, appearing as erosions, fissuring, purpura and ecchymoses; the characteristic sites are the interlabial sulci, labia minora and labia majora, clitoris and clitoral hood, perineum and perianal area, giving the characteristic figure-of-eight shape. In a cohort cited in that review, the labia minora were affected in 87% of women, the perineum in 85%, the clitoris in 72% and the perianal region in 50% (PubMed PMID: 23329078).

Scarring

The 2011 Cochrane review describes how scarring after inflammation may lead to fusion of the labia, narrowing of the vaginal opening and burying of the clitoris if treatment is not started early (PubMed PMID: 22161424). In the Oxford cohort, topical steroid treatment completely reversed the skin changes, with return to normal skin texture and colour, in 58 of 253 patients (23%); moderate or severe scarring occurred less often in girls (PubMed PMID: 15210461). The 2013 review describes surgery in women as limited to associated intraepithelial neoplasia or cancer, or to correcting scarring that interferes with normal function (PubMed PMID: 23329078).

Sexual and Psychological Impact

The EuroGuiderm guideline states that LS may lead to sexual and urinary dysfunction and has “a huge impact on the quality of life of affected patients” (PubMed PMID: 38822578). In a Dutch cohort of 81 adult women diagnosed with vulvar LS in childhood or adolescence (median follow-up 19.5 years), quality of life and sexuality were somewhat affected in 51.9% (PubMed PMID: 37632250). The 2011 Cochrane review lists the effect of treatment on the quality of people’s sex lives among the questions that still need randomized trials (PubMed PMID: 22161424).

Genital LS in Men: BXO and Phimosis

In men, genital LS has historically been called balanitis xerotica obliterans (BXO), a term used in the medical literature alongside “male genital lichen sclerosus” (PubMed PMID: 23329078) (PubMed PMID: 21707769). The 2013 review describes early signs as greyish or bluish-white discolouration of the glans and the inner surface of the foreskin, sometimes with telangiectasia; purpura, bullae, erosions and ulceration may occur, and sclerosis can lead to phimosis (PubMed PMID: 23329078).

Phimosis and Circumcision

In an Australian multicentre study of 611 men circumcised between 2004 and 2018, 313 foreskins were sent for histology, and 199 of these (63.6%) showed LS (PubMed PMID: 35812204). In the London series of 329 men, most were either cured by ultrapotent topical steroid (50–60%) or by circumcision (more than 75%), and the authors reported that effective and definitive management appeared to abrogate the risk of penile squamous cell carcinoma (PubMed PMID: 21707769). The BAD guideline states that “for many patients, circumcision may cure their disease” and that men whose LS-related phimosis does not respond to an ultrapotent topical steroid after 1–3 months are offered referral to an experienced urologist (PubMed PMID: 29313888); the EuroGuiderm guideline states that “complete circumcision may cure LS in males” (PubMed PMID: 38822598). The 2013 review reports a circumcision success rate of 76–100% in men who failed medical treatment or had advanced scarring, notes that LS may recur in the circumcision scar, and reports LS in 10–40% of boys circumcised for phimosis (PubMed PMID: 23329078).

Glans and Meatal Involvement

According to the 2013 review, urethral involvement usually starts at the meatus, and post-inflammatory scarring may lead to meatal and urethral stenosis and obstruction, complications that frequently need surgery. In a review of 522 men cited there, disease was limited to the foreskin and glans in 57%, the meatus was involved in 4% and the urethra in 20% (PubMed PMID: 23329078).

Urethral Extension

In the Australian circumcision cohort, 44 of the men with LS (22.1%) developed urethral stricture disease (PubMed PMID: 35812204). The 2013 review reports that in long-standing disease meatal stenosis may extend along the whole urethra, and that urethroplasty with buccal and/or bladder mucosa grafts may be necessary (PubMed PMID: 23329078).

SCC Risk in Men

In a Danish nationwide registry study, men with histologically verified penile LS had a rate of penile squamous cell carcinoma 15.5 times that of the general population (standardized incidence ratio 15.5, 95% CI 12.0–19.5); the excess rose with longer follow-up and with younger age at LS diagnosis (PubMed PMID: 40251017). The BAD guideline puts the overall rate in men at “probably 4–5% as in women” (PubMed PMID: 29313888). In the Australian circumcision cohort, 1 man with LS (0.5%) developed penile SCC and 1 (0.5%) penile intraepithelial neoplasia (PubMed PMID: 35812204).

Extragenital Lichen Sclerosus

Extragenital involvement is reported in 6% to 20% of patients (PubMed PMID: 27232363); the 2013 review states that only 6% of LS cases are isolated extragenital lesions (PubMed PMID: 23329078).

Sites and Morphology

The 2013 review describes typical extragenital lesions as porcelain-white papules and plaques with follicular delling and hyperkeratosis, and illustrates bluish-white, polygonal papules coalescing into plaques on the wrists (PubMed PMID: 23329078). The Koebner phenomenon (LS in skin already scarred or damaged) is described in the 1999 review (PubMed PMID: 10348006).

Symptoms and Cancer Risk

The 2013 review describes extragenital LS as much less symptomatic than genital LS (PubMed PMID: 23329078). In the Danish penile-LS study, rates of non-penile cancers were mostly close to those of the general population, which the authors read as suggesting that the malignant potential of LS is caused by local factors rather than a general cancer predisposition (PubMed PMID: 40251017).

Treatment

The 2013 review reports that, although topical corticosteroids are regularly used, no randomized trials or case series on them have been published for extragenital LS (PubMed PMID: 23329078). The BAD guideline states: “Consider potent topical steroids, acitretin, methotrexate and phototherapy for people with extragenital LS” (PubMed PMID: 29313888). The EuroGuiderm guideline recommends UV light treatment for extragenital LS while noting that the scientific evidence is limited (PubMed PMID: 38822598). The 2013 review lists extragenital LS with features suggesting an overlap with morphoea as a reason for biopsy (PubMed PMID: 23329078).

Oral LS

In the 2013 review’s comparison table, involvement of the oral mucosa is “very rare” in LS but common in lichen planus (PubMed PMID: 23329078); the 2016 review notes that neighbouring mucous membranes such as the vaginal or oral mucosa are not typically affected (PubMed PMID: 27232363).

Squamous Cell Carcinoma Risk

The 1999 review describes an increased risk of vulvar cancer and links with penile cancer (PubMed PMID: 10348006). The EuroGuiderm guideline states that LS is associated with an increased risk of genital cancer and that “genital LS is often a lifelong disease and needs to be treated long-term” (PubMed PMID: 38822598).

Risk Estimates

In a Dutch registry cohort of 3,038 women diagnosed with lichen sclerosus between 1991 and 2011, the cumulative incidence of vulvar SCC was 6.7%. The 10-year incidence was 18.8% in women with concurrent vulvar intraepithelial neoplasia (VIN) and 2.8% in women without it, and rose with age at lichen sclerosus diagnosis (1.8% under 50, 3% at 50–70, 5.9% at 70 or older) (PubMed PMID: 27257093). The BAD guideline gives the risk of developing malignancy in women as “approximately 3·5–5%” (PubMed PMID: 29313888). Penile cancer risk in men is covered in the section above. Studies summarized in the 2013 review found LS next to the tumour in 33% of 1,287 patients with vulvar SCC (range 7–85% across studies), and identified advanced age and squamous hyperplasia as independent risk factors for vulvar carcinoma in vulvar LS (PubMed PMID: 23329078).

HPV-Independent Pathway

The two pathological pathways to vulvar SCC — one caused by persistent HPV infection and one HPV-independent and often associated with lichen sclerosus — are described on the Vulvar Cancer page. In the Dutch registry, concurrent VIN and age of 70 or older at LS diagnosis remained significant risk factors in adjusted analysis (PubMed PMID: 27257093).

Findings Listed as Reasons for Biopsy

The 2013 review lists these reasons for a biopsy in patients under routine follow-up (PubMed PMID: 23329078):

Treatment Adherence and Cancer Risk

In a prospective single-center cohort of 507 women with biopsy-proven vulvar lichen sclerosus in Sydney, followed for a mean of 4.7 years, biopsy-proven SCC or VIN occurred in none of the 357 patients who adhered to long-term preventive topical corticosteroid treatment, compared with 7 (4.7%) of the 150 who were partially compliant. Symptoms were suppressed in 93.3% vs 58.0%, scarring developed in 3.4% vs 40.0%, and reversible steroid-induced skin atrophy occurred in 1.1% vs 2.0%. The authors concluded that such individualized regimens, with regular long-term follow-up, may modify the course of the disease (PubMed PMID: 26070005). In a French prospective study of 83 women treated with clobetasol propionate, all 8 vulvar SCCs (9.6%) arose in previously untreated or irregularly treated lesions, but the authors noted that the number of seemingly protected patients was too small to be statistically significant (PubMed PMID: 15210462). In the Oxford cohort, SCC developed in 6 women (2.4%) (PubMed PMID: 15210461). The 2013 review states that it is not assured that medical treatment can prevent progression to malignancy, while noting that long-term follow-up studies suggest early diagnosis and treatment with good compliance might lower cancer rates and prevent scarring (PubMed PMID: 23329078).

Diagnosis: Clinical Recognition and Biopsy

The 2016 review lists anogenital itching and clinical features such as erythema, white skin changes (hyperkeratosis and sclerosis) and fissures as signs that should raise suspicion of LS, and states that the diagnosis should be confirmed with a skin biopsy (PubMed PMID: 27232363).

Clinical Diagnosis

A 2005 histopathology review describes vulvar LS as beginning with uncharacteristic symptoms and progressing undiagnosed to atrophy and destructive scarring; its authors advise that patients with persistent vulvar symptoms be biopsied to establish the diagnosis (PubMed PMID: 16178888). In the Oxford cohort, as reported in the 2013 review, a delay in diagnosis of 2 years or less was associated with less scarring at diagnosis (PubMed PMID: 23329078).

When Biopsy Is Described

Beyond the initial diagnosis, the reasons for biopsy during follow-up listed in the 2013 review are given in the cancer-risk section above (PubMed PMID: 23329078). The same review states that when LS does not respond to topical corticosteroids of adequate potency and duration, the diagnosis is reappraised and contact allergy to a constituent of the cream, secondary infection or malignant change are excluded (PubMed PMID: 23329078).

Histological Findings

The 2013 review describes the classic features of advanced uncomplicated LS as hyperkeratosis, epidermal atrophy with flattening of the rete ridges, vacuolar interface changes, loss of elastic fibres, and hyalinization of the lamina propria with an underlying lymphocytic infiltrate, while noting that prominent acanthosis may be a feature, particularly in vulvar LS (PubMed PMID: 23329078). Early LS is harder to recognize: its features are subtle and often more prominent in adnexal structures, with homogenized collagen and wide ectatic capillaries just beneath the basement membrane; biopsies rarely show all features, so serial sections and periodic acid-Schiff staining are described as necessary (PubMed PMID: 16178888).

Key Differential Diagnoses

The 2013 review names the main differential diagnoses as lichen planus, lichen simplex chronicus, vitiligo, immunobullous disorders such as mucous membrane pemphigoid, and vulvar or penile intraepithelial neoplasia. Its comparison of LS with lichen planus (PubMed PMID: 23329078):

Topical Corticosteroids: First-Line Treatment in Guidelines

The EuroGuiderm guideline states that ultrapotent or potent topical corticosteroids “in females and males, adults and children remain gold standard of care for genital LS”, with co-treatment with emollients (PubMed PMID: 38822598); the 2016 review grades early high-potency topical corticosteroid as the treatment of first choice (1/A) (PubMed PMID: 27232363). In the 2011 Cochrane review of 7 randomized trials (249 participants), clobetasol propionate 0.05% was effective against placebo in one trial (participant-rated improvement or remission, risk ratio 2.85, 95% CI 1.45–5.61), mometasone furoate 0.05% improved the clinical grade of phimosis against placebo in another, and neither trial found more adverse reactions than placebo (PubMed PMID: 22161424).

Regimens Described in Guidelines

The BAD guideline’s regimen for adult women is “clobetasol propionate (CP) 0·05% ointment on a regimen for 3 months (once a day for a month, alternative days for a month, twice weekly for a month)”; the same regimen is given for girls, and for men “CP 0·05% ointment once daily for 1–3 months with an emollient as a soap substitute” (PubMed PMID: 29313888). The 2013 review notes that an ointment formulation is usually better tolerated than a cream base, and that several studies found less potent corticosteroids such as mometasone furoate or triamcinolone also effective for vulvar LS (PubMed PMID: 23329078).

Efficacy

In the Oxford cohort (mean follow-up 66 months), response to treatment was recorded in 255 patients: symptoms improved in 244 (96%), with 168 (66%) becoming symptom free and 76 (30%) responding partially, and 11 (4%) responding poorly. Of 253 patients with recorded skin findings, 23% showed total response, 68% partial, 7% minor and 2% poor response. The authors concluded that ultrapotent topical steroid relieves symptoms in most patients and completely reverses the skin changes in approximately one fifth (PubMed PMID: 15210461).

Long-Term Maintenance

The BAD guideline states: “Consider an individualized treatment regimen of topical steroid to maintain disease control and prevent scarring in female patients with ongoing active LS disease despite good compliance” (PubMed PMID: 29313888). In the French study of 83 women treated until complete clinical and histological remission, complete remission was obtained in 54%; the estimated remission rate at 3 years was 72% under age 50, 23% at 50–70 and 0% over 70, and relapse was estimated at 50% at 16 months and 84% at 4 years (PubMed PMID: 15210462). In the Sydney cohort, reversible steroid-induced skin atrophy occurred in 1.1% of compliant and 2.0% of partially compliant patients (PubMed PMID: 26070005). The 2013 review lists the feared adverse effects of long-term topical corticosteroid maintenance as atrophy, striae, rebound reactions, fungal infections, reactivation of HPV and herpes simplex infection, and systemic absorption, while noting that atrophy as an adverse effect of treatment in LS has not been clearly documented because atrophy is part of the disease itself (PubMed PMID: 23329078).

Second-Line and Surgical Treatments

Several other treatments have been studied for LS that does not respond to topical corticosteroids, or where they are not tolerated.

Topical Calcineurin Inhibitors (TCIs)

The guidelines differ. The 2024 EuroGuiderm guideline states that “topical calcineurin inhibitors are second line treatment” (PubMed PMID: 38822598), while the 2018 BAD guideline lists topical calcineurin inhibitors among interventions for which there is currently insufficient evidence to recommend them (PubMed PMID: 29313888). In a double-blind randomized trial in 38 women with biopsy-proven vulvar LS (12 weeks), clobetasol was superior to pimecrolimus in improving inflammation on biopsy (P = .015); itch and burning/pain improved in both groups, with no significant difference between them (PubMed PMID: 21353334). In a double-blind randomized trial of clobetasol propionate 0.05% versus tacrolimus 0.1% over 3 months (55 women analysed), more patients in the clobetasol group (15) had no remaining signs or symptoms, and the authors concluded that clobetasol was significantly more effective (PubMed PMID: 24704090). On safety, the 2013 review reports that the US Food and Drug Administration collated worldwide reports of 19 malignancy-related adverse events with topical tacrolimus and 10 with topical pimecrolimus, three of them in genital LS treated with these drugs; that UK advice has been issued not to apply them to malignant or potentially malignant skin lesions and to keep treatment short term; and that some authors object to their use in a disease with its own malignant potential (PubMed PMID: 23329078).

Less Potent Corticosteroids and Retinoids

The 2013 review reports that less potent topical corticosteroids such as mometasone furoate or triamcinolone were also effective in several studies, and summarizes a randomized, placebo-controlled trial of oral acitretin 35 mg/day for 20 weeks in severe LS resistant to ultrapotent corticosteroids, in which complete response was achieved by 36.4% of the acitretin group versus 6.3% of controls (PubMed PMID: 23329078).

Platelet-Rich Plasma (PRP) and Fat Grafting

These are trial findings from small studies. In a randomized pilot study of 20 women with moderate to severe vulvar LS that had not responded to clobetasol propionate (19 assessed), two injections of nanofat mixed with PRP, 3 months apart, were compared with standard topical corticosteroid; at 1 year there was no significant improvement in vulvar skin elasticity, while the injected group showed significant improvement in symptoms, clinical signs and inflammatory cells on biopsy, with no treatment-related adverse events (PubMed PMID: 35048150). In a randomized study of 40 people with genital LS still symptomatic despite medical treatment, adipose-derived stromal vascular fraction with or without PRP both improved scores at 6 months compared with baseline; the study had no untreated or steroid comparison group, and the combination was less effective in late-stage disease (PubMed PMID: 32888384). The EuroGuiderm treatment guideline abstract does not list PRP or fat grafting among its recommended treatments (PubMed PMID: 38822598).

Laser Therapy

Laser trials have reached different results. In a double-blind, sham-controlled trial of 40 women (37 analysed), five fractionated CO2 laser treatments did not change the histopathology score significantly compared with sham, and the authors concluded that fractionated CO2 laser “is not an effective monotherapy treatment” for vulvar LS; the laser’s manufacturer supplied the laser and part of the funding (PubMed PMID: 33957648). In a single-center randomized trial of 52 women, fractionated CO2 laser improved Skindex-29 quality-of-life scores more than clobetasol propionate at 6 months, but after stratification the difference was seen only in women previously treated with steroids (PubMed PMID: 33957642). In an open-label randomized trial of 245 women, three courses of low-density fractional CO2 laser produced greater symptom improvement at 3 months than a 3-month tapered clobetasol propionate regimen (median change in burn-itch-pain score −8 vs −5) (PubMed PMID: 42208069). The EuroGuiderm guideline states that laser treatment “is under investigation, and it can currently not be recommended for the treatment of LS” (PubMed PMID: 38822598).

Photodynamic Therapy and Systemic Agents

The 2013 review describes photodynamic therapy for genital LS, and phototherapy for extragenital LS, as options in rare cases that do not respond to the treatments above, and topical and systemic retinoids as possibly useful in selected cases (PubMed PMID: 23329078). The EuroGuiderm guideline reports that treatment with biologics has been described only in single cases (PubMed PMID: 38822598).

Surgical Treatments

In women, the 2013 review describes surgery as limited to associated intraepithelial neoplasia or cancer, or to scarring that restricts function (PubMed PMID: 23329078). In boys and men whose LS does not remit after steroid treatment, the 2016 review states that circumcision is indicated (evidence grade 3/D) (PubMed PMID: 27232363), and the EuroGuiderm guideline recommends a surgical intervention when standard treatment fails in males (PubMed PMID: 38822598). Outcomes of circumcision and urethral surgery are described in the section on men above.

Monitoring and Long-Term Follow-Up

The 1999 review states that patients “should be kept under long-term review” (PubMed PMID: 10348006). The BAD guideline suggests two follow-up visits for women after the first consultation, “one at 3 months to assess response to treatment” and a second 6 months later, with the same timing for men and children (PubMed PMID: 29313888). In the Sydney cohort, patients were followed up at least annually (PubMed PMID: 26070005).

Monitoring Goals

The outcomes followed in the long-term studies above are symptom control, scarring and fusion of structures, intraepithelial neoplasia and cancer, and adverse effects of treatment (PubMed PMID: 26070005). Follow-up is often incomplete: in the Dutch cohort of women diagnosed in childhood, fewer than half (45%) reported regular check-ups, 56% reported symptoms in the past year (31% of whom were not under surveillance), and 20% had not known of their childhood diagnosis before the study (PubMed PMID: 37632250).

Self-Examination

The FIGO cancer report’s statements on self-examination by women with lichen sclerosus are reported on the Vulvar Cancer page.

Clinical Assessment Tools

Trials have measured LS with different instruments, including a histopathology scale and the Clinical Scoring System for Vulvar Lichen Sclerosus (CSS) (PubMed PMID: 33957648), the Skindex-29 quality-of-life questionnaire (PubMed PMID: 33957642), and a burn-itch-pain (BIP) score from 0 to 30 (PubMed PMID: 42208069).

The Course in Children After Puberty

In a prospective case series from Sydney (Smith and Fischer), 12 girls who developed LS before puberty were followed into adolescence or young adulthood. Three achieved complete remission sustained for three or more years, all before menarche; nine (75%) still had active LS at puberty and continued to need maintenance treatment after menarche, and six of the 12 had significant disturbance of vulvar architecture. The authors concluded that the idea that prepubertal LS resolves at puberty “would appear not to be true in the majority of patients” (PubMed PMID: 20199450). A retrospective study of 21 girls cited in the 2013 review found that definite symptoms and signs persisted after puberty in 76% (PubMed PMID: 23329078). The BAD guideline states that “although childhood LS often improves at puberty, there may be cases that persist into adulthood” (PubMed PMID: 29313888). In the Dutch cohort, 56% of women diagnosed as girls reported symptoms in the past year, at a median of 19.5 years after diagnosis (PubMed PMID: 37632250).

Psychosexual Support

Sexual function has been measured in treatment studies: the 2013 review reports that Female Sexual Distress Scale scores fell from 29 to 15 with clobetasol propionate ointment and from 27 to 21 with pimecrolimus cream (PubMed PMID: 23329078). In the Dutch childhood-onset cohort, quality of life and sexuality were somewhat affected in 51.9% and correlated with recent symptoms (PubMed PMID: 37632250). Decisions about treatment and follow-up belong with a clinician.

Key Research Papers

Key peer-reviewed studies on lichen sclerosus pathogenesis, diagnosis, and treatment. Each PMID link opens the study on PubMed.

  1. Powell JJ, Wojnarowska F. Lichen sclerosus. Lancet. 1999;353(9166):1777–1783. — PubMed PMID: 10348006
  2. Cooper SM, et al. Does treatment of vulvar lichen sclerosus influence its prognosis? Arch Dermatol. 2004;140(6):702–706. — PubMed PMID: 15210461
  3. Oyama N, et al. Autoantibodies to extracellular matrix protein 1 in lichen sclerosus. Lancet. 2003;362(9378):118–123. — PubMed PMID: 12867112
  4. Bleeker MC, et al. Lichen sclerosus: incidence and risk of vulvar squamous cell carcinoma. Cancer Epidemiol Biomarkers Prev. 2016;25(8):1224–1230. — PubMed PMID: 27257093
  5. Lee A, Bradford J, Fischer G. Long-term management of adult vulvar lichen sclerosus: a prospective cohort study of 507 women. JAMA Dermatol. 2015;151(10):1061–1067. — PubMed PMID: 26070005
  6. Renaud-Vilmer C, et al. Vulvar lichen sclerosus: effect of long-term topical application of a potent steroid on the course of the disease. Arch Dermatol. 2004;140(6):709–712. — PubMed PMID: 15210462
  7. Cheng S, Kirtschig G, Cooper S, et al. Interventions for erosive lichen planus affecting mucosal sites. Cochrane Database Syst Rev. 2012;(2):CD008092. — PubMed PMID: 22336835 (Editorial note: this review concerns lichen planus, a differential diagnosis, not lichen sclerosus.)
  8. Morrel B, et al. Long-term consequences of juvenile vulvar lichen sclerosus: a cohort study of adults with a histologically confirmed diagnosis in childhood or adolescence. Acta Obstet Gynecol Scand. 2023;102(11):1469–1478. — PubMed PMID: 37632250
  9. Te B, Julien D, Mar K, Liu R, Kirshen C. Pediatric lichen sclerosus and non-accidental trauma: a systematic review of distinguishing features and co-occurrence. Pediatr Dermatol. 2026;43(2):323–329. — PubMed PMID: 41461155
  10. Regauer S, Liegl B, Reich O. Early vulvar lichen sclerosus: a histopathological challenge. Histopathology. 2005;47(4):340–347. — PubMed PMID: 16178888
  11. Lewis FM, et al. British Association of Dermatologists guidelines for the management of lichen sclerosus, 2018. Br J Dermatol. 2018;178(4):839–853. — PubMed PMID: 29313888
  12. Fistarol SK, Itin PH. Diagnosis and treatment of lichen sclerosus: an update. Am J Clin Dermatol. 2013;14(1):27–47. — PubMed PMID: 23329078
  13. Kirtschig G. Lichen sclerosus — presentation, diagnosis and management. Dtsch Arztebl Int. 2016;113(19):337–343. — PubMed PMID: 27232363
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Curated PubMed topic searches:

  1. PubMed: LS ECM-1 autoantibodies
  2. PubMed: VLS clobetasol
  3. PubMed: LS SCC risk
  4. PubMed: LS in children
  5. PubMed: BXO penile LS
  6. PubMed: LS tacrolimus
  7. PubMed: LS autoimmune
  8. PubMed: LS long-term

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